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1. 北京大学第三医院中医科
2. 北京中医药大学针灸推拿学院
3. 河北大学中医学院
4. 浙江省人民医院康复医学科
纸质出版日期:2022
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吕巧巧, 张莉, 李霞, 等. 电针“委中”对腰多裂肌损伤大鼠铁代谢紊乱的保护作用[J]. 针刺研究, 2022,47(12):1073-1079.
Lü Qiao-qiao, ZHANG Li, LI Xia, et al. Effect of electroacupuncture of “Weizhong” (BL40) on iron metabolism disorder in rats with lumbar multifidus muscle injury[J]. Acupuncture research, 2022, 47(12): 1073-1079.
吕巧巧, 张莉, 李霞, 等. 电针“委中”对腰多裂肌损伤大鼠铁代谢紊乱的保护作用[J]. 针刺研究, 2022,47(12):1073-1079. DOI: 10.13702/j.1000-0607.20211277.
Lü Qiao-qiao, ZHANG Li, LI Xia, et al. Effect of electroacupuncture of “Weizhong” (BL40) on iron metabolism disorder in rats with lumbar multifidus muscle injury[J]. Acupuncture research, 2022, 47(12): 1073-1079. DOI: 10.13702/j.1000-0607.20211277.
目的:观察腰多裂肌损伤后铁代谢紊乱及氧化应激水平,探讨电针“委中”是否通过对铁代谢紊乱的调节作用来调节氧化应激,从而促进损伤腰多裂肌的修复。方法:将SD大鼠随机分为正常组、模型组、电针组,每组6只。采用一次性注射0.5%布比卡因(BPVC)制备腰多裂肌损伤大鼠模型。造模后24 h开始电针双侧“委中”
30 min/次,1次/d
治疗2 d。HE染色法观察腰多裂肌形态变化;普鲁士蓝染色法观察腰多裂肌组织铁小粒数量;Western blot法检测腰多裂肌谷胱甘肽合成酶(GSS)蛋白表达量;荧光定量PCR法检测腰多裂肌铁调节蛋白1(IRP1)、铁转运蛋白(Fpn)、铁蛋白重链1(FTH1)、谷胱甘肽过氧化物酶4 (GPX4) mRNA的表达水平;生化法检测腰多裂肌组织谷胱甘肽(GSH)、丙二醛(MDA)含量。结果:与正常组比较,模型组腰多裂肌肌纤维大片坏死、断裂,伴有大量炎性细胞浸润,铁小粒增多,肌纤维间隙增大;电针组肌纤维损伤较模型组减轻,铁小粒减少。与正常组比较,模型组腰多裂肌铁代谢相关指标IRP1 mRNA表达水平升高(P<0.001)
Fpn、FTH1 mRNA表达水平降低(P<0.001);与模型组比较,电针组腰多裂肌IRP1 mRNA表达水平降低(P<0.001)
Fpn、FTH1 mRNA表达水平升高(P<0.05
P<0.01)。与正常组比较,模型组腰多裂肌氧化应激相关指标GSS蛋白表达量、GPX4 mRNA表达水平、GSH含量降低(P<0.001)
MDA含量升高(P<0.001);与模型组比较,电针组腰多裂肌GPX4 mRNA表达水平、GSH含量升高(P<0.05
P<0.01)
MDA含量降低(P<0.001)。结论:BPVC致大鼠腰多裂肌损伤后,损伤局部组织出现铁代谢紊乱,电针“委中”可作用于IRP1、Fpn、FTH1
恢复铁代谢平衡,缓解腰多裂肌组织氧化损伤,促进大鼠腰多裂肌损伤后的修复。
Objective To observe the effect of electroacupuncture(EA) of “Weizhong”(BL40) on the disorder of iron metabolism and the level of oxidative stress after lumbar multifidus muscle injury(LMMI)
so as to explore its mechanisms underlying promoting the repair of LMMI. Methods Male SD rats were randomly divided into normal
model and EA groups(6 rats in each group). The LMMI model was established by injecting 0.5% bupivacaine(BPVC) solution(400 μL) into the lumbar multifidus muscle with the syringe-needle close to the spinous process(L4-L5). Twenty-four hours after successful establishment of the model
EA(2 Hz/15 Hz
2 mA) was applied to bilateral BL40 for 30 min
once a day for 2 days. Histopathological changes of the multifid muscle were observed under microscope after H.E. staining
and the iron granules in the multifid muscle tissue observed after Prussian blue staining. The expression of glutathione synthase(GSS) was detected by Western blot
and the expressions of iron regulatory protein 1(IRP1)
ferroportin(Fpn)
ferritin heavy chain 1(FTH1
iron metabolism-related proteins) and gluta-thione peroxidase 4(GPX4
functions in protecting cells against detrimental lipid peroxidation and governing a novel form of regulated necrotic cell death
called ferroptosis) mRNAs were detected by quantitative real-time PCR. The contents of glutathione(GSH) and malondialdehyde(MDA) were measured by biochemical methods. Results H.E. staining showed large areas of necrosis and breakage of muscle fibers
disordered arrangement of muscle fibers
widened muscle cell space
accompanying with a large number of inflammatory cell infiltration in the multifidus muscle tissue of the model group
which was relatively milder in the EA group. Outcomes of Prussian blue staining showed that compared with the normal group
there were more iron particles in the multifidus muscle tissue and enlarged muscle fiber gaps
which was also milder in the EA group. Compared with the normal group
the expression level of IRP1 mRNA and content of MDA were significantly increased(P<0.001)
the expression levels of Fpn
FTH1 and GPX4 mRNAs and GSS protein
and the content of GSH were considerably decreased(P<0.001) in the model group. In comparison with the model group
the increase of IRP1 mRNA expression and MDA content
as well as the decrease of Fpn
FTH1 and GPX4 mRNAs expressions and GSH content were reversed in the EA group(P<0.001
P<0.05
P<0.01). Conclusion EA of BL40 has a protect effect in BPVC-induced injury of lumbar multifidus muscle in rats
which may be related to its functions in improving iron metabolism to reduce oxidative damage by regulating expression of IRP1
Fpn and FTH1.
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